Despite years of intensive investigation that has been made in understanding prostate cancer, it remains one of the major men’s health issues and the leading cause of death worldwide. It is now ascertained that prostate cancer emerges from multiple spontaneous and/or inherited alterations that induce changes in expression patterns of genes and proteins that function in complex networks controlling critical cellular events. It is now accepted that several innate and adaptive immune cells, including T- and B-lymphocytes, macrophages, natural killer cells, dendritic cells, neutrophils, eosinophils, and mast cells (MCs), infiltrate the prostate cancer. All of these cells are irregularly scattered within the tumor and loaded with an assorted array of cytokines, chemokines, and inflammatory and cytotoxic mediators. This complex framework reflects the diversity in tumor biology and tumor-host interactions. MCs are well-established effector cells in Immunoglobulin-E (Ig-E) associated immune responses and potent effector cells of the innate immune system; however, their clinical significance in prostate cancer is still debated. Here, these controversies are summarized, focusing on the implications of these findings in understanding the roles of MCs in primary prostate cancer. 1. Introduction Human carcinogenesis is a dynamical process that depends on a high number of variables and its regulation can be presented through multiple spatial and temporal scales [1–4]. Despite the advances in our genomic and cellular knowledge [5], prostate cancer remains one of the major public health problems throughout the world [6, 7]. It is important that it is recently gaining recognition being highly heterogeneous and therefore encompassing a wide range of clinical behaviors. It is evident that prostate cancer is underpinned by a complex array of gene alterations that affect molecular, cellular, and supracellular processes [5, 8–10]. It is also ascertained that solid tumors, including prostate cancer, are commonly infiltrated by a high number of innate and adaptive immune cells [11–16]. All of them are variably scattered within the tumor and loaded with an assorted array of cytokines, chemokines, and inflammatory and cytotoxic mediators [17–19]. This complex network reflects the diversity in tumor biology and tumor-host interactions. It has been recognized that inflammation plays a role in the development and progression of solid tumors although it still remains unclear whether aggressive disease caused increased inflammation or inflammation caused aggressive disease [20, 21].
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